1. Field of Invention
The present invention relates to a method of preventing and/or treating diabetes type 2, also, it relates to a method of augmenting Glut4 phosphorylation and Glut4 translocation to a target cell membrane to enhance insulin signal in a signal transduction pathway; further, it relates to a simplified and inexpensive process of obtaining extract and thereafter selectively, its active n-butanol fraction and active molecule Lupinoside PA (LPA4), useful in preventing and/or treating diabetes type 2; and lastly, a pharmaceutical composition thereof.
2. Background of the Present Invention
Type 2 insulin-resistant diabetes mellitus, an insidious disease, accounts for more than 95% of diabetic cases. This heterogeneous disorder is increasing in epidemic proportions, its world wide frequency is expected to grow more than six percent per anum1,2. The disease is primarily expressed in the form of hyperglycemia due to defects in glucose disposal into skeletal muscle, fat and liver as they become less responsive or resistant to insulin3,4. Large number of evidences has been accumulated that hold free fatty acids (FFAs) responsible for insulin inaction. Elevated FFAs in circulation is associated with impaired insulin function and is commonly linked with obesity and type 2 diabetes5-7. Rising of plasma FFA concentrations through lipid infusion causes insulin resistance in rat and human skeletal muscle7-9. Incubation of isolated muscle strips or cultured muscle cells with FFAs or lipoprotein lipase expression in skeletal muscle reduces insulin-mediated glucose uptake6-12. These reports suggest that greater deposition of lipid in insulin sensitive tissues promotes insulin inaction and resistance. FFA induced impairment of insulin activity appears to be associated with insulin signaling defects. Lowering of glucose transport by FFA is linked to inhibition of insulin-stimulated IRS-1 phosphorylation and IRS-1 associated phosphatidylinositol-3-phosphate kinase (PI3K) activation13-15. Thiazolidinedione (TZD) treatment reduces circulating FFAs that oppose insulin actions in target tissues improving insulin activity16-18. By inducing the glycerol kinase gene expression in adipocytes through the activation of PPARγ, TZD augments glycerol incorporation into triglyceride thus reduces FFA secretion from the adipocyte and that helps insulin sensitizations19.